Abstract
Leptin is a key biological marker related to energy balance and development of diabetes
and cardiovascular diseases. Its levels are increased in populations with a high degree
of the metabolic syndrome. Life history of evolution has, however, largely taken place
under the ecological context of hunting and gathering. In this study, we explored
whether the first steps of transition to sedentary agriculture involve a change of
body composition, plasma leptin concentration, and markers of the metabolic syndrome.
A total of 59 healthy Shuar Amerindian women living in 5 isolated communities in the
Ecuadorian Amazonian rain forest were examined. Women (n = 33) from the largest and
oldest community, Yuwientsa, who are more dependent on agriculture had higher fat
mass (11.7 ± 3.3 v 14.5 ± 4.0 kg; P = .023) but the same body mass index (24.1 ± 2.7 v 23.1 ± 2.8 kg/m2; not significant [NS]) and lean body mass (41.0 ± 5.0 v 40.2 ± 6.2 kg; NS) than women (n = 26) from the 4 traditional hunter/gather settlements.
Furthermore, women from Yuwientsia had higher leptin (5.5 ± 3.1 v 4.1 ± 2.7 ng/mL; P = .021) and plasma insulin levels (49.8 ± 37.4 v 35.5 ± 12.7 pmol/L; P = .013). Homeostasis model assessment (HOMA) values (8.8 ± 4.8 v 6.1 ± 2.2; P = .004) and plasma triglyceride levels (2.3 ± 1.0 v 1.7 ± 0.6 mmol/L; P = .025) as markers of the metabolic syndrome were also increased in the Yuwientsa
population. Mean plasma glucagon concentrations were not different between the groups.
We conclude that body fat and levels of insulin and leptin are higher in the population
more dependent on agriculture for living. In fact, the leptin concentrations from
the 4 hunter/gather communities are the lowest mean value ever reported from a population
of healthy females. As there are no genetic or biologic differences between the Shuar
Indians from the 5 communities, we hypothesize that behavioral responses to a changing
environment may be the key to the development of the metabolic syndrome and elevated
plasma leptin concentrations.
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Article info
Publication history
Accepted:
April 9,
2004
Received:
January 22,
2004
Footnotes
☆Supported by Grant No. 6834 from the Swedish Research Council, Albert Pahlsson Foundation, Swedish Diabetes Association, and Stiftelsen för forskning inom diabetes och kärlsjukdom.
Identification
Copyright
© 2004 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
